Postprandial hyperlipidemia with accumulation of remnant lipoproteins is usually a common

May 16, 2019 by Gavin Berry·Comments Off on Postprandial hyperlipidemia with accumulation of remnant lipoproteins is usually a common

Postprandial hyperlipidemia with accumulation of remnant lipoproteins is usually a common metabolic disturbance associated with atherosclerosis and vascular dysfunction, particularly during chronic disease states such as obesity, the metabolic syndrome and, diabetes. pharmacological interventions could result in a further decrease of cardiovascular mortality and morbidity. This paper will provide an update on current concepts concerning the relationship between postprandial lipemia, inflammation, vascular function, and therapeutic options. 1. Introduction Atherosclerosis is the main cause of death in the world [1]. Classical risk factors such as smoking, hypertension, fasting hyperlipidemia, insulin resistance, increased body fat mass, and unfavourable body fat distribution are strongly interrelated and can often be found in one and the same subject. Subjects with fasting hypertriglyceridemia usually have elevated postprandial lipids due to the close correlation of fasting and postprandial triglycerides (TG) [2]. Postprandial lipemia has gained interest because of recent reports showing that nonfasting TG independently predict the risk for atherosclerosis [3, 4] and are possibly even stronger predictors of cardiovascular disease (CVD) than fasting TG [3, 5]. Atherosclerosis is considered a low-grade chronic inflammatory disease [6], and both the postprandial phase and chronic disease says such as the metabolic syndrome are associated with increased inflammation. This paper outlines recent developments in the understanding of postprandial inflammation and its relationship with vascular function, metabolic diseases, and lifestyle behaviour. 2. Metabolism of Postprandial Lipemia Dietary fat is usually assimilated in the intestine and Carboplatin cost secreted into lymph by enterocytes in TG-rich chylomicrons. Once in the blood circulation, chylomicrons rapidly undergo hydrolysis to produce cholesterol-dense lipoprotein remnants which are taken up by the liver [7, 8]. After a fatty meal, exogenous fatty acids are delivered to the liver by chylomicron remnants and may then be reassembled and returned to the blood in very low-density lipoproteins (VLDL) [9]. The hypertriglyceridemia observed postprandially is due to raised concentrations of chylomicrons, VLDL, and their respective remnants, collectively known as triglyceride-rich lipoproteins (TRLs). People in the Western world are nonfasting for most of the day, consequently leading to a continuous challenge of the endothelium by atherogenic lipoprotein remnants [10, 11]. The exogenous chylomicrons and endogenously produced VLDL share the same metabolic pathway, for example, endothelium-bound lipoprotein lipase (LPL), which hydrolyzes TG into glycerol and fatty acids. In the postprandial phase, due to limited LPL availability, competition at the level of this enzyme will occur resulting in accumulation of TRLs. This competition is most likely when fasting hypertriglyceridemia is present. The increased levels Carboplatin cost of free fatty acids (FFAs) as a result of a hypercaloric diet are regarded as one of the important etiologic components of the metabolic syndrome, type 2 diabetes (T2DM), and obesity [12, 13]. 3. Residual Risk of Cardiovascular Disease after LDL Cholesterol Lowering Based on results from large clinical trials, lipid management for reducing the risk for CVD has been typically focused on reducing LDL-C by statin therapy [14C18]. Despite aggressive LDL-C lowering by statin therapy, approximately two-thirds of all CVD events remain. These residual events appear to be independent of the LDL-C and in recent years have gained momentum as a concept of residual risk of CVD. Interestingly, statins do reduce postprandial lipemia and also AURKA have an effect on match, but they do not impact TG sufficiently to be of Carboplatin cost clinical relevance in hypertriglyceridemic conditions [2, 19C22]. Interestingly, this residual risk has been found Carboplatin cost to be greater for treated patients with diabetes or the metabolic syndrome than in untreated patients without these conditions [23, 24]. One could interpret these observations to infer that statin therapy, resulting in LDL-C lowering, does not necessarily bring the relative CVD risk in patients suffering from diabetes and metabolic syndrome to the level of nondiabetics and patients without metabolic syndrome. Consequently, the current model we Carboplatin cost propose is usually that the residual risk hypothesis of atherosclerosis is not just dependent on circulating concentrations of LDL-C but is usually equally dependent on remnant lipoprotein concentrations and perturbations in the arterial vessel wall that influence the rate of arterial lipoprotein retention. The potential impact of the residual risk.